Severe ethylene glycol intoxication with marked lactate and osmolar gaps leading to acute kidney injury: a case report

Ethylene glycol (EG) is a common constituent of automotive antifreeze and industrial solvents. Following ingestion, it is metabolized by alcohol dehydrogenase to glycoaldehyde and subsequently to glycolic acid, glyoxylic acid, and oxalic acid. These metabolites cause high anion gap metabolic acidosis and calcium oxalate crystal deposition, leading to acute kidney injury (AKI) and neurological impairment. We describe the case of a 65-year-old man with chronic alcohol use who presented to the emergency department 48 h after ingesting a ‘strong mixed drink’ for inebriation. On admission, he was confused, tachypneic, and dehydrated. Laboratory studies revealed severe metabolic acidosis (pH 6.86), a markedly elevated anion (31.6 mmol/L) and lactate (138.5 mg/dL) gaps, hyperkalemia, and rising creatinine, in the absence of shock or hypoperfusion. A family member provided the ingested product (ISOTECH-ITCOOLANT), which contained monoethylene glycol. Immediate management included intravenous bicarbonate, 10% ethanol as an antidote, thiamine and folic acid supplementation, and urgent hemodialysis. Calculated and measured osmolarity, osmolar gap, lactate gap, and urinary oxalate confirmed EG poisoning. This case highlights the importance of early recognition and prompt initiation of antidotal therapy and extracorporeal removal in EG intoxication, as delayed presentation may result in severe renal and neurological injury despite appropriate treatment.